Different quantitative apoptotic traits in coronary atherosclerotic plaques from patients with stable angina pectoris and acute coronary syndromes
- 1Division of Cardiology, Istituto Clinico Humanitas, Milan, Italy. marcolrossi@hotmail.com
- 0Division of Cardiology, Istituto Clinico Humanitas, Milan, Italy. marcolrossi@hotmail.com
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View abstract on PubMed
Summary
This summary is machine-generated.Acute coronary syndrome (ACS) plaques show increased apoptosis due to specific gene activation, unlike stable angina plaques which maintain cell repair. This suggests apoptosis contributes to plaque instability in ACS.
Area Of Science
- Cardiovascular Biology
- Molecular Biology
- Pathology
Background
- Apoptosis, or programmed cell death, may destabilize atherosclerotic coronary plaques by weakening the fibrous cap.
- This study investigated if apoptosis is quantitatively increased in unstable atherosclerotic plaques.
Purpose Of The Study
- To test the hypothesis that apoptosis is quantitatively increased in unstable atherosclerotic plaques.
- To compare gene expression related to apoptosis in stable versus unstable coronary plaques.
Main Methods
- Analyzed apoptotic gene expression (e.g., BAX, CASP1, FAS, P53) in coronary plaques from stable angina and acute coronary syndromes (ACS) patients.
- Utilized RNA extraction, cDNA amplification, DNA laddering, in situ RT-PCR, and immunocytochemistry.
- Confirmed findings with Western blotting.
Main Results
- Pro-apoptotic genes were significantly upregulated (P<0.001) in ACS plaques compared to stable plaques.
- Anti-apoptotic genes were significantly upregulated (P<0.001) in stable angina plaques.
- DNA laddering confirmed end-point apoptosis in ACS plaques, with mRNA localized to vascular smooth muscle cells.
Conclusions
- ACS plaques exhibit a commitment to apoptosis via specific gene regulation.
- Stable angina plaques maintain cell homeostasis and repair mechanisms.
- Apoptosis plays a key role in the destabilization of atherosclerotic plaques in ACS.
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